Demonstration of 6-phosphogluconolactonase activity in Drosophila melanogaster using a null allele of 6-phosphogluconate dehydrogenase

1978 ◽  
Vol 16 (9-10) ◽  
pp. 1023-1029 ◽  
Author(s):  
M. Beatrice Hughes ◽  
John C. Lucchesi
Keyword(s):  
Drosophila Melanogaster ◽  
Null Allele ◽  
Phosphogluconate Dehydrogenase

scholarly journals LETHAL EFFECTS OF LOW AND "NULL" ACTIVITY ALLELES OF 6-PHOSPHOGLUCONATE DEHYDROGENASE IN DROSOPHILA MELANOGASTER

Genetics ◽  
1975 ◽  
Vol 79 (3) ◽  
pp. 451-457
Author(s):  
Glenn C Bewley ◽  
John C Lucchesi
Keyword(s):  
Drosophila Melanogaster ◽  
Embryonic Development ◽  
Enzymatic Activity ◽  
Null Allele ◽  
Developmental Rate ◽  
Lethal Effects ◽  
Homozygous Condition ◽  
Phosphogluconate Dehydrogenase ◽  
Relative Viability ◽  
Low Activity

ABSTRACT EMS-induced "null" and low activity alleles for 6-phosphogluconate dehydrogenase were characterized with respect to enzymatic activity, relative viability, fertility, and the effective lethal phase. It was determined that flies hemizygous and homozygous for the low activity allele, Pgd  -, possessed a depressed developmental rate, diminished viability, and loss of female fertility. Heterozygotes for Pgd  - and a deficiency for Pgd  + were lethal. The "null" activity allele demonstrated a lethal phenotype in both the hemizygous and homozygous condition. The effective lethal phase for the "null" allele occurs during late embryonic development (20-22 hr).

scholarly journals Genetic and Molecular Characterization of sting, a Gene Involved in Crystal Formation and Meiotic Drive in the Male Germ Line of Drosophila melanogaster

Genetics ◽  
1999 ◽  
Vol 151 (2) ◽  
pp. 749-760 ◽  
Author(s):  
Armin Schmidt ◽  
Gioacchino Palumbo ◽  
Maria P Bozzetti ◽  
Patrizia Tritto ◽  
Sergio Pimpinelli ◽  
...  
Keyword(s):  
Amino Acids ◽  
Drosophila Melanogaster ◽  
Null Allele ◽  
Germ Line ◽  
Meiotic Drive ◽  
P Element ◽  
Crystal Formation ◽  
Male Sterile ◽  
Male Sterile Mutation

Abstract The sting mutation, caused by a P element inserted into polytene region 32D, was isolated by a screen for male sterile insertions in Drosophila melanogaster. This sterility is correlated with the presence of crystals in spermatocytes and spermatids that are structurally indistinguishable from those produced in males carrying a deficiency of the Y-linked crystal (cry) locus. In addition, their morphology is needle-like in Ste+ flies and star-shaped in Ste flies, once again as observed in cry– males. The sti mutation leads to meiotic drive of the sex chromosomes, and the strength of the phenomenon is correlated with the copy number of the repetitive Ste locus. The same correlation is also true for the penetrance of the male sterile mutation. A presumptive sti null allele results in male sterility and lethal maternal effect. The gene was cloned and shown to code for a putative protein that is 866 amino acids long. A C-terminal domain of 82 amino acids is identified that is well conserved in proteins from different organisms. The gene is expressed only in the germline of both sexes. The interaction of sting with the Ste locus can also be demonstrated at the molecular level. While an unprocessed 8-kb Ste primary transcript is expressed in wild-type males, in X/Y homozygous sti males, as in X/Y cry– males, a 0.7-kb mRNA is produced.

scholarly journals Interacting proteins identified by genetic interactions: a missense mutation in alpha-tubulin fails to complement alleles of the testis-specific beta-tubulin gene of Drosophila melanogaster.

1989 ◽  
Vol 9 (3) ◽  
pp. 875-884 ◽  
Author(s):  
T S Hays ◽  
R Deuring ◽  
B Robertson ◽  
M Prout ◽  
M T Fuller
Keyword(s):  
Drosophila Melanogaster ◽  
Missense Mutation ◽  
Null Allele ◽  
Genetic Interaction ◽  
Structural Proteins ◽  
Interacting Proteins ◽  
Tubulin Gene ◽  
Beta Tubulin ◽  
Gene Encoding ◽  
Alpha Tubulin

In this paper we demonstrate that failure to complement between mutations at separate loci can be used to identify genes that encode interacting structural proteins. A mutation (nc33) identified because it failed to complement mutant alleles of the gene encoding the testis-specific beta 2-tubulin of Drosophila melanogaster (B2t) did not map to the B2t locus. We show that this second-site noncomplementing mutation is a missense mutation in alpha-tubulin that results in substitution of methionine in place of valine at amino acid 177. Because alpha- and beta-tubulin form a heterodimer, our results suggest that the genetic interaction, failure to complement, is based on the structural interaction between the protein products of the two genes. Although the nc33 mutation failed to complement a null allele of B2t (B2tn), a deletion of the alpha-tubulin gene to which nc33 mapped complemented B2tn. Thus, the failure to complement appears to require the presence of the altered alpha-tubulin encoded by the nc33 allele, which may act as a structural poison when incorporated into either the tubulin heterodimer or microtubules.

scholarly journals The ash-1, ash-2 and trithorax genes of Drosophila melanogaster are functionally related.

Genetics ◽  
1989 ◽  
Vol 121 (3) ◽  
pp. 517-525 ◽  
Author(s):  
A Shearn
Keyword(s):  
Drosophila Melanogaster ◽  
Null Allele ◽  
Homeotic Gene ◽  
Bithorax Complex ◽  
Substantial Evidence ◽  
Genetic Tests ◽  
Recessive Lethal ◽  
The Third ◽  
Sex Combs

Abstract Mutations in the ash-1 and ash-2 genes of Drosophila melanogaster cause a wide variety of homeotic transformations that are similar to the transformations caused by mutations in the trithorax gene. Based on this similar variety of transformations, it was hypothesized that these genes are members of a functionally related set. Three genetic tests were employed here to evaluate that hypothesis. The first test was to examine interactions of ash-1, ash-2 and trithorax mutations with each other. Double and triple heterozygotes of recessive lethal alleles express characteristic homeotic transformations. For example, double heterozygotes of a null allele of ash-1 and a deletion of trithorax have partial transformations of their first and third legs to second legs and of their halteres to wings. The penetrance of these transformations is reduced by a duplication of the bithorax complex. The second test was to examine interactions with a mutation in the female sterile (1) homeotic gene. The penetrance of the homeotic phenotype in progeny from mutant mothers is increased by heterozygosis for alleles of ash-1 or ash-2 as well as for trithorax alleles. The third test was to examine the interaction with a mutation of the Polycomb gene. The extra sex combs phenotype caused by heterozygosis for a deletion of Polycomb is suppressed by heterozygosis for ash-1, ash-2 or trithorax alleles. The fact that mutations in each of the three genes gave rise to similar results in all three tests represents substantial evidence that ash-1, ash-2 and trithorax are members of a functionally related set of genes.

Interacting proteins identified by genetic interactions: a missense mutation in alpha-tubulin fails to complement alleles of the testis-specific beta-tubulin gene of Drosophila melanogaster

1989 ◽  
Vol 9 (3) ◽  
pp. 875-884
Author(s):  
T S Hays ◽  
R Deuring ◽  
B Robertson ◽  
M Prout ◽  
M T Fuller
Keyword(s):  
Drosophila Melanogaster ◽  
Missense Mutation ◽  
Null Allele ◽  
Genetic Interaction ◽  
Structural Proteins ◽  
Interacting Proteins ◽  
Tubulin Gene ◽  
Beta Tubulin ◽  
Gene Encoding ◽  
Alpha Tubulin

In this paper we demonstrate that failure to complement between mutations at separate loci can be used to identify genes that encode interacting structural proteins. A mutation (nc33) identified because it failed to complement mutant alleles of the gene encoding the testis-specific beta 2-tubulin of Drosophila melanogaster (B2t) did not map to the B2t locus. We show that this second-site noncomplementing mutation is a missense mutation in alpha-tubulin that results in substitution of methionine in place of valine at amino acid 177. Because alpha- and beta-tubulin form a heterodimer, our results suggest that the genetic interaction, failure to complement, is based on the structural interaction between the protein products of the two genes. Although the nc33 mutation failed to complement a null allele of B2t (B2tn), a deletion of the alpha-tubulin gene to which nc33 mapped complemented B2tn. Thus, the failure to complement appears to require the presence of the altered alpha-tubulin encoded by the nc33 allele, which may act as a structural poison when incorporated into either the tubulin heterodimer or microtubules.

Interspecific hybridization between Drosophila species group melanogaster sibling species: isozymic patterns and reproductive relationships

Genome ◽  
1989 ◽  
Vol 32 (1) ◽  
pp. 146-154 ◽  
Author(s):  
G. N. Goulielmos ◽  
S. N. Alahiotis
Keyword(s):  
Drosophila Melanogaster ◽  
Sex Ratio ◽  
Interspecific Hybrids ◽  
Aldehyde Oxidase ◽  
Species Group ◽  
Fitness Components ◽  
Phosphogluconate Dehydrogenase ◽  
Evolutionary Changes ◽  
Fertile Hybrids ◽  
Male Genital

In spite of previous consensus that no F1 fertile hybrids (of both sexes) could be produced between any mating combination of Drosophila melanogaster, D. simulans, and D. mauritiana, the present data indicate that such hybrids were obtained. Thus, some crosses between D. mauritiana females and D. simulans or D. melanogaster males yield F1 fertile hybrids (of both sexes) which have been named Masi (or Masi-2 and Masi-3) and Mame, respectively. Electrophoretic studies, using the species-diagnostic genes for 6-phosphogluconate dehydrogenase, alcohol dehydrogenase, and aldehyde oxidase (6-Pgd, Adh, and Aldox, respectively), were used to investigate the hybrid status, taking into consideration (i) their reproductive relationships, (ii) the coexistence of electromorphs from different species in the same hybrid, within the same generation, and (iii) the expression of the above electromorphs in the hybrids as well as in progeny from backcrosses, where unexpected irregularities and abnormalities were observed. These interspecific hybrids have been kept in our laboratory (as stocks) for 50 generations, to date, and have also been tested for various characteristics that contributed to the verification of their hybrid status (mating abilities, enzyme activities, hybrid sex ratio, the morphology of male genital arches and other fitness components). The finding of major genetic phenomena (e.g., allozymic repression) in these hybrid genomes gives some idea of the nature of events that could be associated with strong evolutionary changes, thus controlling speciation processes.Key words: Drosophila, electrophoresis, electromorphs, interspecific hybrids.

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